Week 13 lectures 1-3 skeletal neuro muscular junction Flashcards
how fast can action potentials travel
120 metres/sec
how many neurons does the human brain have
100 billion
what is needed to open up vesicles
calcium ions , action potential
what is the neuromuscular junction
the synapse between a neurone and a skeletal muscle fibre
how many steps are involved in the release of a transmitter and what are they and how can they be influenced
there are 5 steps
Synthesis
storage
release
activation
inactivation
They are influenced by drugs and toxins resulting in resulting in either an increase or a decrease of transmission
how can drugs enhance synaptic transmission and explain
1) direct stimulation of the post-synaptic receptors by
a) the natural transmitter
b) analogues
2) indirect action via:
a) increased transmitter release
b) inhibition of transmitter removal
how can drugs inhibit synaptic transmission and explain
1)blocking synthesis, storage, or release from the presynaptic neuron.
2) Blocking post synaptic receptors
what are the names of drugs that directly act on receptors
agonists and antagonists
what are agonists and describe them entirely
agonists are drugs, hormones, or transmitters which can bind to specific receptors and initiate a conformational change in the receptor resulting in a biological response.
what are the two important properties of agonists and describe them
affinity (the ability of agonists to bind to receptors) and
efficacy (the ability of an agonist, once bound to a receptor, to initiate a biological response.
what is an antagonist
antagonists bind to receptors but do not activate them
They posses affinity but not efficacy
they block receptors activation by the agonists
what is a competitive antagonist
it competes with the agonist for the “agonists binding site” on the receptor.
what is the neurotransmitter at the neuromuscular junction (NMJ)
acetylcholine
how are synapses classified
according to the transmitter released from the presynaptic neurone
what does it mean if the transmission is cholinergic
the presynaptic neuron synthesises and releases acetylcholine (ACh)
What are the 2 classes of cholinoceptors and describe them
1) Nicotinic cholinoceptors (activated by ACh or the tobacco alkaloid nicotine but not the muscarine.
2) Muscarinic cholinoceptors activated by ACh or the fungal alkaloid muscarine but not nicotine
how is fast transmission mediated
transmitter-gated ion channels
how many subunits are there
5
beta
gamma
delta
2 alpha
what flows throw the subunits into the cell
sodium ion cations flow in and potassium out
what happens when an agonist binds to the receptor
induces a rapid conformational change to open the channel
how quick can signalling happen
milliseconds
what does mepps stand for
Miniature end plate potentials
what happens when ACh is released from a single vesicle
many nicotinic ACh receptors are activated
what happens when the ACh receptors are activated
the associated cation channels open and the Na+ ions flux into the muscle fibre to cause a local depolarisation at the endplate region (ie. a mepp)
what does electron microscopy reveal
vesicle in the apparent act of exocytosis
what does a black widow spider venom(alpha Latrotoxin, aka -a-LTX) do
it influences spontaneous transmitter release
what is exocytosis
vesicle fusion
what is endocytosis
recovery of vesicular membrane after fusion
what would you expect to see on a mepp recording with a control and with the black widow venom
control: miniature spikes as the transmitter is being released as normal
venom: massive releases in the ACh neurotransmitter causing muscle spasms and massive spikes in the mepp recording
what would happen after being bitten by the black widow venom
depletion of vesicles
inhibition of endocytosis
distended terminal
paralysis
list the simplified model of fast synaptic transmission
1) Presynaptic action potential
2) A synchronous Ca2+ influx via voltage-gated Ca2+ channels
3) Many vesicles undergo exocytosis releasing a large cloud of acetylcholine
4) Activation of many nicotinic acetylcholine receptors
5) This causes a large depolarization of endplate region of muscle cell (an epp)
6) If the depolarization is large enough it activates postsynaptic voltage-gated sodium channels to initiate an action potential
